EV71抑制Ⅰ型干扰素信号通路中ISGF3的核转位  

EV71 inhibits nuclear translocation of ISGF3 in type Ⅰ interferon signaling pathway

作　　者：刘颖[1] 赵兴卉[1] 张晓鹏[1] 于蕊[1] 吴诗坡[1] 张哲[1] 戴萌萌[1] 付玲[1] 侯利华[1] 

机构地区：[1]军事医学科学院生物工程研究所,北京100071

出　　处：《军事医学》2013年第10期734-736,744,共4页Military Medical Sciences

摘　　要：目的探讨肠道病毒71型(enterovirus 71,EV71)感染对Ⅰ型干扰素信号通路中核转位复合物干扰素刺激基因因子3(ISGF3)核转位的影响。方法 Western印迹检测VR1432感染VeroE6对干扰素诱导的STAT1和STAT2磷酸化的影响。将pEGFP-C1-STAT1重组质粒转染Vero E6细胞,随后进行EV71感染以及IFN-α2b刺激,将细胞进行亚细胞分离检测ISGF3的核转位情况。结果 VR1432以感染复数(MOI)为1感染Vero E6细胞后未影响干扰素刺激的STAT1和STAT2的磷酸化;亚细胞分离后Western印迹检测磷酸化的STAT1,结果显示VR1432感染后,p-STAT1在细胞核内表达水平明显降低,说明EV71感染抑制了p-STAT1的核转位。结论 EV71感染抑制Ⅰ型干扰素信号通路中ISGF3(STAT1/STAT2/IRF9)的核转位,从而影响干扰素效应途径中抗病毒蛋白的表达。Objective To explore the effect of enterovirus 71 （EVT1） infection on the interferon-stimulated gene factor 3 （ISGF3） nuclear translocation in type I IFN signaling pathway. Methods The phosphorylation levels of STAT1 and STAT2 in Vero E6 cells were detected by Western blotting in the presence or absence of VR1432 infection after IFN-ct treatment. Vero E6 cells were transfected with pEGFP-C1-STAT1 and subsequently infected with VR1432 virus. The cells were treated with IFN-ot2b before harvest. Nuclear-cytosol extraction was conducted to examine the translocation of ISGF3 in EV71-infected cells. Results Western blotting showed that VR1432 infected at multiplicity of infection（MOI） of 1 did not alter the total IFN-induced phosphorylation of STAT1, but the phosphorylation of STAT1 was significantly reduced in the nuclei of VR1432-infected cells after IFN-a2b treatment. Conclusion VR1432 virus inhibits the nuclear translocation of IFN-induced ISGF3.

关 键 词：肠道病毒71型 ISGF3 干扰素I型 信号通路 核转位 

分 类 号：R373[医药卫生—病原生物学]